Advancements in the molecular biology of growth factors, growth factor receptors, and cell/matrix receptors and the appreciation that these proteins have contextual and combinational effects on cell function have allowed investigators to form rather elaborate hypotheses as to how wound repair processes may evolve and regress. The recent availability of probes for these proteins and their effector functions has given the investigator tools with which to test these hypotheses and to search for mechanisms by which dysregulated repair may lead to nonhealing wounds or fibrotic disease. Gradually the external signals that modulate cell phenotype during tissue repair and the intracellular controls of this phenotypic modulation will become elucidated. By drawing investigators together from diverse fields, it is hoped that this meeting will speed our understanding of wound repair and thereby facilitate beneficial intervention in nonhealing wounds and fibrotic disease.